title: Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure.
abstract: BACKGROUND
  There is limited knowledge about atrial myocyte Ca(2+) handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca(2+) handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction.
  
  
  RESULTS
  Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca(2+) amplitude, decreased SR Ca(2+) content, and slower Ca(2+) transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca(2+) ATPase activity, increased Na(+)/Ca(2+)-exchanger activity and increased diastolic Ca(2+) leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca(2+) handling in HF.
  
  
  CONCLUSIONS
  Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca(2+) handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.
authors.affiliation: K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Anne Berit
authors.initials: AB
authors.lastname: Johnsen
authors.forename: Morten
authors.initials: M
authors.lastname: Høydal
authors.forename: Ragnhild
authors.initials: R
authors.lastname: Røsbjørgen
authors.forename: Tomas
authors.initials: T
authors.lastname: Stølen
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisløff
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D002316:Cardiotonic Agents / Q000494:pharmacology; D004558:Electric Stimulation; D005081:Exercise Therapy; D005260:Female; D006325:Heart Atria / Q000473:pathology*; D032342:Muscle Cells / Q000187:drug effects / Q000502:physiology*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy*; D010101:Oxygen Consumption; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D002110:Caffeine; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium